Page 958 - Problem-Based Feline Medicine

950 PART 11 CAT WITH AN ABNORMAL GAIT

causes continuous bleeding from sites including
SNAKEBITE ENVENOMATION WITH
AUSTRALIAN SNAKES** trauma sites, gastrointestinal tract, and lungs mani-
festing as hematemesis, hematuria, hemoptosis, etc.
● Coagulant manifestations often precede neurotoxin
Classical signs
signs.
● Australian snake venoms are ● Antitoxin effectively blocks the clotting mechanism
predominately neurotoxic and usually activation.
strongly coagulant.
Rhabdomyolysis (tiger, mulga, small-eyed) manifests
● Usually no local reaction at the site of
as myoglobinuria.
venom injection.
● Generalized muscle weakness and dilated Hemolysins (taipan, black) cause intravascular haemol-
pupils that are poorly responsive to light ysis and may manifest as jaundice, anemia, hemoglo-
are features. binuria and perhaps kidney tubular necrosis.
● Complete flaccid paralysis is a common
Hyaluronidase in the venom is responsible for the rapid
finding.
entry of the venom into the circulation.
● Vomiting and rapid respiration are present
in 30% of cases. The lack of local reaction at the bite site is probably due
to the low quantity of proteolytic enzymes in Australian
snake venom.
Pathogenesis
Clinical signs
Bites from Brown snakes (Pseudonaja sp.), Tiger
snakes (Notechnis scutatus), Taipan (Oxyuranus There is marked variation in type and severity of signs but
s. scutellatus) and Death Adders (Acanthophis antarcti- flaccid paralysis and dilated pupils that are poorly
cus) can cause ataxia, paralysis and dilated pupils. responsive are consistent findings, that is, neurological
signs predominate.
Neurotoxins act specifically at the neuromuscular
junction to paralyze all skeletal voluntary muscle. Onset is usually sudden.
Postsynaptic neurotoxins (tiger, brown, taipan, death Dilated pupils, ataxia to paresis, trembling, flaccid
adder) cause a non-depolarizing block of neuromuscular paralysis, vomiting, diarrhea, respiratory distress, hypo-
transmission by occupying acetylcholine receptors on thermia, weakness, pallor, jaundice, dark urine and bleed-
the motor endplate. Flaccid paralysis ensues and death ing from multiple sites may all be present.
is possible from respiratory failure.
Less commonly there is a history of initial collapse fol-
Presynaptic neurotoxins (tiger, brown, taipan) block lowed by apparent full recovery followed by a steady
acetylcholine release into the neuromuscular junction progression of clinical signs over the ensuing hours,
after depolarization. This action is delayed, becoming which may take from 5 minutes to 24 hours in the cat.
evident after 30–60 minutes.
The bite site may not be found unless there is bleeding
Increased catecholamine release (stress, exercise, nerve from the site.
stimulation) enhances the rate of intoxication whereas
Multiple bite sites usually result in the introduction of
low temperatures delay this process.
large quantities of venom.
Antitoxin cannot reverse presynaptic binding of
toxin. Diagnosis
The clotting mechanism is activated via initiation of A history of being bitten by a snake and finding the
the conversion of prothrombin to thrombin and fib- snake greatly aids diagnosis, but more often the bite is
rinogen to fibrin (tiger, brown, taipan, black). This unobserved.